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Background: Aerobic training can be defined as any physical exercise that increases the heart rate and enhances the body's intake of oxygen long enough to benefit the condition of body. Running, cycling, and swimming are examples of aerobic activities. This type of exercise optimises immune functions. Recently several experimental findings suggested that the regular swimming training increase immune response, but there have been very few reports which compare warm water exercise with cold water exercise in spleen lymphocytes. Methods: This study was designed to examine the effects of regular swimming training on Index, the number of lymphocytes, proliferative activity and production of reactive oxygen species (ROS) by splenocytes in BALB/c mice. Thirty six mice (6 week old) were performed 10 weeks of regular swimming training and they were divided into 6 groups according to the regular swimming training (CRG: control resting group, CEG: control exercise group, WRG: warm water trained resting group, WEG: warm water trained exercise group, CORG: cold water trained resting group, COEG: cold water exercise group). Analytical items were weight change, spleen index, the number of lymphocytes, proliferative activity and production of ROS. All data were expressed as mean and standard deviation by using SPSS package program (ver. 10.0). Results: The swimming training significantly decreased body weight, and increased spleen index, the number of lymphocytes and proliferative activity in the presence or absence of Con A and LPS added conditions. For the WRG and CORG, the quantity of ROS from splenocytes was higher than CRG, whereas, ROS by spleen lymphocytes was lower following 90 min acute exercise stress. Conclusion: These results suggested that the swimming training not only increases the number of lymphocytes but also increases proliferative activity by splenocytes in vitro.
Purpose: Dickkopf-1 (DKK-1) is a Wnt/β-catenin signaling pathway inhibitor. We investigated whether DKK-1 is related to progressionin hepatocellular carcinoma (HCC) cells and HCC patients. Materials and Methods: In vitro reverse-transcription polymerase chain reaction (RT-PCR), wound healing assays, invasion assays,and ELISAs of patient serum samples were employed. The diagnostic accuracy of the serum DKK-1 ELISA was assessed usingreceiver operating characteristic (ROC) curves and area under ROC (AUC) analyses. Results: RT-PCR showed high DKK-1 expression in Hep3B and low in 293 cells. Similarly, the secreted DKK-1 concentration in the culture media was high in Hep3B and low in 293 cells. Wound healing and invasion assays using 293, Huh7, and Hep3B cells showed that DKK-1 overexpression promoted cell migration and invasion, whereas DKK-1 knock-down inhibited them. When serum DKK-1 levels were assessed in 370 participants (217 with HCC and 153 without), it was significantly higher in HCC patients than in control groups (median 1.48 ng/mL vs. 0.90 ng/mL, p<0.001). The optimum DKK-1 cutoff level was 1.01 ng/mL (AUC=0.829; sensitivity 90.7%; specificity 62.0%). Although DKK-1 had a higher AUC than alpha-fetoprotein (AFP) and des-gamma-carboxy prothrombin (DCP) (AUC=0.829 vs. 0.794 and 0.815, respectively), they were statistically similar (all p>0.05). When three biomarkerswere combined (DKK-1 plus AFP plus DCP), they showed significantly higher AUC (AUC=0.952) than single marker, DKK-1 plus AFP, or DKK-1 plus DCP (all p<0.001). Conclusion: DKK-1 might be a key regulator in HCC progression and a potential therapeutic target in HCC. Serum DKK-1 could complement the diagnostic accuracy of AFP and DCP.
Background: Epstein-Barr virus associated gastric lymphoepithelioma-like carcinoma (LELC) is characterized by the intensive infiltration of lymphoid cells, the presence of EBV,and the better prognosis over typical adenocarcinoma. Thus,it was assumable that viral latent proteins may be responsible for the recruitment of a certain T cell repertoire to EBV-associated gastric carcinoma. Methods: To examine above possibility, EBV gene expression in gastric carcinoma tissues and usage of TCR among the tumor infiltrating lymphocytes were analyzed. Results: EBV specific DNA and EBERs RNA were detected in 4 out of 30 patients. RT-PCR analysis revealed that all 4 of EBV-positive tumor tissues expressed EBNA1 mRNA and BARTs and LMP2a was detected only one sample out of 4. However, the EBNA2 and LMP-1transcripts were not detected in these tissues. CD8+ T cells were the predominant population of infiltrating lymphocytes in the EBV-positive gastric carcinoma. According to spectra type analysis of infiltrating T cells, 10 predominant bands were detected by TCR Vβ CDR3 specific RT-PCR from 4EBV-positive tumor tissues. Sequence analysis of these bands revealed oligoclonal expansion of T cells. Conclusion:These findings suggest that clonally expanded T cells in vivo might be a population of cytotoxic T cells reactive to EBV-associated gastric carcinoma.
Tsutsugamushi disease, an infectious disease by Rickettsia(R.) tsntsugamushi, is characterized by eschar, fever and rash. Eschar caused by chigger bite, is pre sent on 47 94% of patients with documented R. tsutsugamushi. We recently noticed one case of R. tsutsugamushi infection. Patient had fever, heaclache, lymphadenopathy, erythematous maculopapules and eschar. The R. tsu tsugamushi was isolated from serum of the patient. Histopathologic findings of eschar show epidermal ulceration overlying a zone of coagulative necrosis of upper dermis and necrotizing vasculitis. Electron microscopic findings of endothelial cells of capillary show rickettsia with cell division.
Purpose: The aim of this study was to investigate whether the peroxisomal proliferator-activated receptor gamma (PPARγ) ligand troglitazone in combination with photodynamic therapy (PDT) enhances the apoptotic response of DLD-1 colon cancer cells. Materials and Methods: The effects of troglitazone, PDT, and troglitazone in combination with PDT on cell viability and apoptosiswere assessed in DLD-1 cells. Cell viability and proliferation were evaluated using the tetrazolium-based MTT assay, and apoptosis was evaluated via cell staining with propidium iodide (PI) and annexin V-FITC. The levels of pro-caspase-3 were measuredvia Western blot analyses. Results: Treatment of troglitazone and PDT induced the growth retardation and cell death of DLD-1 cells in a dose-dependent manner, respectively. The combination treatment significantly suppressed cell growth and increased the apoptotic response of DLD-1 and resulted in apoptosis rather than necrosis, as shown by PI/annexin V staining and degradation of procaspase-3. Conclusion: These results document the anti-proliferative and apoptotic activities of PDT in combination with the PPARγ ligand troglitazone and provide a strong rationale for testing the therapeutic potential of combination treatment in colon cancer.